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A panel of p16 INK4A , MIB1 and p53 proteins can distinguish between the 2 pathways leading to vulvar squamous cell carcinoma
Author(s) -
Hoevenaars Brigiet M.,
van der Avoort Irene A.M.,
de Wilde Peter C.M.,
Massuger Leon F.A.G.,
Melchers Willem J.G.,
de Hullu Joanne A.,
Bulten Johan
Publication year - 2008
Publication title -
international journal of cancer
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.475
H-Index - 234
eISSN - 1097-0215
pISSN - 0020-7136
DOI - 10.1002/ijc.23857
Subject(s) - immunohistochemistry , vulvar intraepithelial neoplasia , vulvar carcinoma , vulvar cancer , pathology , cancer research , biology , carcinoma , medicine , vulva
Two pathways leading to vulvar squamous cell carcinoma (SCC) exist. The expression of proliferation‐ and cell‐cycle‐related biomarkers and the presence of high‐risk (hr) HPV might be helpful to distinguish the premalignancies in both pathways. Seventy‐five differentiated vulvar intra‐epithelial neoplasia (VIN)‐lesions with adjacent SCC and 45 usual VIN‐lesions (32 solitary and 13 with adjacent SCC) were selected, and tested for hr‐HPV DNA, using a broad‐spectrum HPV detection/genotyping assay (SPF 10 ‐LiPA), and the immunohistochemical expression of MIB1, p16 INK4A and p53. All differentiated VIN‐lesions were hr‐HPV‐ and p16‐negative and in 96% MIB1‐expression was confined to the parabasal layers. Eighty‐four percent exhibited high p53 labeling indices, sometimes with parabasal extension. Eighty percent of all usual VIN‐lesions were hr‐HPV‐positive, p16‐positive, MIB1‐positive and p53‐negative. Five (of seven) HPV‐negative usual VIN lesions, had an expression pattern like the other HPV‐positive usual VIN lesions. In conclusion, both pathways leading to vulvar SCC have their own immunohistochemical profile, which can be used to distinguish the 2 types of VIN, but cannot explain differences in malignant potential. © 2008 Wiley‐Liss, Inc.